Protective effect of selenomethionine on intestinal injury induced by T- 2 toxin

T-2 toxin is the most toxic as a type A trichothecenes, which could contaminate grains, especially in wheat and corn. It can cause immune suppression, neurotoxicity, the apoptosis of cells and even induce tumorigenesis. Recent studies have indicated that selenium (Se) have protective effect against mycotoxins-induced toxicity. The present studies was designed to investigate the protective role of Selenomethionine (SeMet) on T-2 toxin-induced toxicity in rabbit's jejunum. 50 New Zealand rabbits were divided into five group (Control group, T-2 group, low-dose Se + T-2 group, medium-dose + T-2 group and high-dose Se + T-2 group). New Zealand rabbits were orally administered with SeMet (0.2, 0.4 and 0.6 mg/kg, Adding diet) for 21 days. On 17th days, each group began to take 0.4 mg/kg of T-2 toxin orally every day for 5 days. We found that rabbit exposed to T-2 toxin could increase the levels of ROS, and decrease activities of antioxidant enzymes and the expression of Occludin and ZO-1. In addition, T-2 toxin could trigger jejunal inflammatory response and enhance the expression of IL-1β, IL-6 and TNF-α. After SeMet pretreatment, our results indicated that Se attenuated the T-2 toxin-induced oxidative stress, decreasing the level of ROS, MDA and enhancing the activity of SOD and GSH-Px. Moreover, SeMet can alleviate jejunal inflammatory response, and protect the integrity of the intestinal barrier through up-regulating the expression of ZO-1 and Occludin. In the present research, supplementation of 0.2 mg/kg SeMet in the diet could effectively alleviate the T-2 toxin poisoning in rabbits.